Transcript The Aging Eye - Nebraska Optometric Association

Dr. Desinee Drakulich
Disclosure Statement
I have no affiliation or get paid by any of the
companies who’s products I discussed in
this lecture.
The Aging Process
Aging is a continuous, complex, and dynamic process that begins with birth and
ends with death. And unless we die in our early years, each of us will grow old
and experience the effects of the aging process.
Unfortunately, no reliable measurement exists that allows us to determine the
biological age of humans. The most promising, however, are in the realm of
genetic and cellular functioning. Two biological phenomena appear related to
the aging process:
•Accumulation of waste products in the cells
•Loss of elasticity of the connective body tissue
The human eye undergoes all the same aging changes as the rest of the body.
Today we will cover:
The normal and abnormal effects of aging on the eye from the lids to the
optic nerve (front to back)
Structures that will be covered:
• Eyelids
Vitreous
• Tear Film
Retina
• Sclera
Optic Nerve
• Cornea
Eye Muscles
• Iris
• Angle
• Lens
Eyelids
Dermatochalasis - redundant and lax eyelid skin and muscle is known as
dermatochalasis. Dermatochalasis is a common finding seen in elderly
persons and occasionally in young adults. Gravity, loss of elastic tissue in the
skin, and weakening of the connective tissues of the eyelid frequently
contribute to this lax and redundant eyelid tissue. These findings are more
common in the upper eyelids but can be seen in the lower eyelids as well.
Dermatochalasis can be a functional or cosmetic problem for the patients.
When functional, dermatochalasis frequently obstructs the superior visual
field. In addition, patients may note ocular irritation, entropion of the upper
eyelid, ectropion of the lower eyelid, blepharitis, and dermatitis. When
cosmetic, patients note a fullness or heaviness of the upper eyelids, "bags" in
the lower eyelids, and wrinkles in the lower eyelids and the lateral canthus.
Ectropion
Ectropion is the turning out of the eyelid (usually the lower eyelid) so that
the inner surface is exposed.
Ectropion is usually caused by the aging process and the weakening of the
connective tissue of the eyelid, which causes the lid to turn out.
Dermatochalasis
Treatment the treatment of dermatochalasis is surgical (blepharoplasty).
The following medical treatments may be appropriate:
•Dermatochalasis patients with blepharitis may benefit from lid hygiene and
topical antibiotics.
•Dermatochalasis patients with dermatitis may benefit from topical steroid
ointment.
•Dermatochalasis patients with dry eyes should be treated with the
appropriate topical lubricant. In addition, placement of temporary collagen
punctal plugs, permanent punctal plugs, or punctal cautery may be
considered in patients with a history of dry eye or a physical examination
consistent with dry eye. These measures may be used preoperatively to
further evaluate the patient prior to embarking upon surgery.
Mechanism of MGD
Androgen deficiency, such as occurs during menopause, aging, Sjögren's
syndrome, complete androgen insensitivity syndrome and the use of antiandrogen medications, leads to meibomian gland dysfunction, altered lipid
profiles in meibomian gland secretions, decreased tear film stability and
evaporative dry eye.
Meibomian Gland Dysfunction
The meibomian glands are located in the eyelids. Secretions from these
glands comprise the lipid (oily) layer of the tear film which is so crucial in
preventing rapid evaporation of the tears. Failure of these glands to produce
or secrete oil - due to chronic blockage, thickening of the meibum, etc. will
affect the quality and stability of the tear film, which in turn will produce
classic dry eye symptoms even in people whose dry eye test results appear
normal.
As we age oil viscosity increases and the loss of functioning meibomian
glands increases.
Tear Film
The tear film is composed of three layer.
Lipid layer – produced by meibomian glands in the upper and lower eyelids.
Aqueous layer – produced by the lacrimal gland.
Mucin layer – produced by the goblet cells in the conjuctiva.
Meibomian Gland Dysfunction
Treatment:
Warm compresses
Digital massage
Lid hygine
Artificial Tears – Systane, Optive, Thera Tears, Genteal
Topical antibiotics – Azasite
Oral antibiotics – Doxycycline
Topical Steroids – FML, Pred Forte, Lotemax
Lipid Layer
Produced by meibomian glands in the eyelids.
Function is to decrease evaporation rate of aqueous tears and give a smooth
blinking surface.
Decreased production secondary to meibomian gland dysfunction and/or
damaged meibomian glands.
Aqueous Layer
Usually caused by inflammatory changes associated with autoimmune
disorders Sjogrens, SLE and Rheumatoid Disease.
Not necessarily associated with aging.
Produced by the lacrimal gland.
Aqueous Deficiency / Goblet Cell
Damage
Inflammation of the lacrimal gland can also increase with age. This
inflammation can reduce to quantity of aqueous tears produced. This is
most commonly treated with Restasis.
Restasis is a cyclosponin drop use to decrease inflammation and stimulate
the lacrimal gland to increase tear production.
Goblet cell damage from sun exposure or autoimmune disorders can
decrease mucin production decreasing tear film stability. Often difficult to
treat may need surgical mucous membrane grafting.
Aging changes to the Sclera
Thins
Density
Color
Water retention
Uveal Sclera Output decreases
Increase in growths
Normal Aging Changes of the Cornea
Over time, the cornea becomes flatter
Thinner
Slightly less transparent
Its refractive index increases
Descemet's membrane becomes thicker. Increases from 3 u at birth to 10 u in
adults as a result of the increased thickness of its posterior non-banded
zone.
Occasional peripheral endothelial gutatta, sometimes known as HassallHenle bodies, can form with age.
Age-related attrition of corneal endothelial cells results in a loss of about
100,000 cells during the first 50 years of life, from a cell density of about
4,000 cells/mm2 at birth to a density of 2500 - 3000 cells/mm2 in older
adults. The average rate of endothelial cell density decrease throughout
adult life is approximately 0.6% per year.
Epithelial Layer
It acts as a barrier to protect the cornea, resisting the free flow of fluids from
the tears, and prevents bacteria from entering the epithelium and corneal
stroma.
Epithelial Layer is made up of 4 types of cells
Surface – squamous cells
Second – prickle cells
Third – wing cells
Fourth – columnar basal cells
Constantly undergoing mitosis.
Bowman’s Layer
a tough layer that protects the corneal stroma, consisting of a similar
irregularly arranged collagen fibers
Epithelial Basement Membrane
Dystrophy
Corneal map-dot-fingerprint dystrophy is by far the most common corneal
dystrophy and is named from the appearance of its characteristic slit lamp
findings. Map-dot-fingerprint dystrophy is also known as Cogan’s dystrophy,
Cogan microcystic epithelial dystrophy, epithelial basement membrane
dystrophy, and anterior basement membrane dystrophy
Stromal Layer
A thick, transparent middle layer, consisting of regularly arranged collagen
fibers along with sparsely distributed interconnected keratocytes, which are
the cells for general repair and maintenance.
Changes in the morphology of the collagen fibers in the stroma can cause an
irregularity to the fibers causes a hazy in the stroma that can effect the
clarity of the cornea and visual acuity.
Arcus Senilis
Is a white or gray opaque ring in the corneal margin (peripheral corneal
opacity), white ring around the iris. It is quite commonly present in the
elderly. It can also appear earlier in life as a result of high cholesterol.
It results from cholesterol deposits in or hyalinosis of the corneal stroma and
may be associated with ocular defects or with familial hyperlipidemia.
Descemet’s Membrane
Descemet's membrane is the basement membrane that lies between the
stroma, and the endothelial layer of the cornea. It is composed of a different
kind of collagen.
Fuch’s Endothelial Dystrophy
Fuchs endothelial dystrophy is characterized by an asymmetrical, bilateral,
slowly progressive edema of the cornea in elderly patients.
The root cause of the condition is a slowly progressive formation of guttate
lesions between the corneal endothelium and the Descemet membrane.
Guttata
Bumps that form between Descemet’s Membrane and the Endothelial layer.
Signs that the endothelial pumps are not working correctly.
Pupil myosis
The pupil becomes smaller and less responsive to variations in light.
Because the pupil controls the amount of light that reaches the retina, agerelated changes to the pupil may affect vision in many ways. First, as the
pupil decreases in diameter, seeing well in dim light becomes harder. In
addition, the less able the pupil is to adjust to varying light conditions, the
less tolerable glare becomes and the more difficult it is to adapt from
darkness to bright light or vice versa. This means as you get older, you may
need more time to adjust to changing levels of illumination, such as going
from bright sunshine into a dimly lit room or restaurant.
Iris Atrophy
A thinning of the iris secondary to loss of pigment and elasticity of the iris.
Floppy Iris Syndrome
A prolapse and constriction of the iris during cataract surgery that can cause
serious complications.
Caused by alpha -1- antagonist (a specific drug type).
Major drug of concern is Flomax ( a prostate medication)
Angle Narrowing
Two significant causes:
Cataract formation – cataract enlarges the size of the lens with can decrease
the space in the anterior chamber.
Flattening of the cornea secondary to a decrease in collagen fiber elasticity.
Lens
The lens of the eye begins to lose elasticity.
In the same way that losing flexibility in tendons and muscles makes it more
difficult for the body to move, losing lens elasticity also makes it harder for
the lens to bend in order to focus on closely held objects. This loss of
focusing power, or lens accommodation, is known as presbyopia.
Age-Related Cataracts
A cataract is simply an opacification of the crystalline lens of the eye.
There are really three types of age-related cataracts:
Nuclear cataract - which is located in the center of the lens, the nucleus, is
most commonly seen as it forms. It is said that the cause of this cataract is
due to changes in the protein structure as we age.
Cortical cataract - starts of on the outside of the lens and slowly extends to
the center. This cataract is common for the elderly and diabetics.
Posterior Subcapsular cataracts - begins at the back of the lens. People who
have a higher risk of developing this form of cataract are: people with
diabetes, high farsightedness, retinitis pigmentosa or those taking high
doses of steroids.
Vitreous
The vitreous is a thick, transparent substance that fills the center of the eye.
It is composed mainly of water and comprises about 2/3 of the eye's volume,
giving it form and shape. The viscous properties of the vitreous allow the eye
to return to its normal shape if compressed.
In children, the vitreous has a consistency similar to an egg white. With age
it gradually thins and becomes more liquid. The vitreous is firmly attached to
certain areas of the retina. As the vitreous thins, it separates from the retina,
often causing floaters.
Vitreous Syneresis
Floaters are deposits of various size, shape, consistency, refractive index,
and motility within the vitreous, which is normally transparent. They may be
of embryonic origin or acquired due to degenerative changes of the vitreous
or retina. Floaters are visible because of the shadows they cast on the retina
or their refraction of the light that passes through them, and can appear
alone or together with several others in one's field of vision. They may
appear as spots, threads, or fragments of cobwebs, which float slowly before
the observer's eyes.
Asteroid Hyalosis
Calcium deposit that form in the vitreous. Patient is usually asymptomatic
with little to no vision loss.
Posterior Vitreous Detachment
occurs when the vitreous, a gel-like substance attached to the retina in the
back of the eye, shrinks and pulls away from the retina.
PVD
Posterior Vitreous Detachment
Symptoms – flashing light and/or floating spots with little or no vision loss
and little or no visual field loss.
Symptoms – patients often describe it as a cobweb or flys in their vision.
What can happen to the eye- generally nothing, however, in rare causes as
the vitreous detaches from the retina it can tear or pull the retina off.
Signs of a retinal detachment – increase in flashing lights, increase in
floating spots, a decrease in vision and a curtain or vale in the vision.
Aging Changes in the Retina
Photoreceptor and Ganglion Cells
Oxidative stress. Cellular damage caused by reactive oxygen intermediates
(ROIs) such as free radicals, peroxides, and single oxygen species. Can also occur
from the presence of polyunsaturated fats and continuous exposure to light.
Cell number reduction. Rod cells (periphery) normally reduce by approximately
30% with age, leading to diminished night vision. Number of cone cells (central)
normally remains fairly stable. Number of rod cells is approximately 120 million.
Number of cone cells is 6.3 to 6.8 million.
Bruch's membrane
Drusen. Accumulation of lipids and photoreceptor cell waste material. Soft
drusen can lead to neovascularization. Hard drusen is not necessarily a
precursor of macular degeneration.
Choroid
Reduced blood flow. Possibly caused by accumulation of waste and retinal
pigment epithelium (RPE) ischemia. Can lead to malnutrition of the
photoreceptor cells.
Macular Degeneration
Age-related macular degeneration (AMD) is a chronic condition that causes
central vision loss. It affects millions of Americans. In fact, it is a leading
cause of blindness in people 60 and older. The older you are, the greater your
chance of being affected.
AMD symptoms include blurriness, wavy lines, or a blind spot.
You may also notice visual distortions such as:
• Straight lines or faces appearing wavy
• Doorways seeming crooked
• Objects appearing smaller or farther away
Two forms of Macular Degeneration – Dry and Wet
Risk Factors
Age
Smoking
Light colored eyes
Family History
Poor diet
UV exposure
Vascular System
Hypertension and Hypercholesterol
Vascular narrowing
Cholesterol plaques
Optic Atrophy
Blood pressure and cholesterol problems can cause a stroke in the eye.
Ocular Muscles
Decomposition of ocular muscles can cause diplopia secondary to ocular
deviation.
Thank you for your attention
Any questions?
Thank you to the
NOA.
References
Kaiser, Friedman, and Pineda. “The Massachusetts Eye and Ear Infirmary
Illustrated Manual of Ophthalmology” Second Edition. 1998
Onofrey, Skorin Jr, and Holdeman. “Ocular Therapeutics Handbook, A
Clinical Manual” Second Edition. 1998
National Health Institute. “ Facts about Macular Degeneration”
www.nei.nih.gov
AMDF: American Macular Degeneration Foundation www.macular.org
National Health Institute. “Facts about Glaucoma” www.ncbi.nlm.nih.gov